[酒精性心肌病和绝缘应激大鼠血管反应性和内源性血管收缩剂受体表达]。

L M Kozhevnikova, I B Tsorin, A I Varkov, V N Stolyaruk, M B Vititnova, L G Kolik, I F Sukhanova, S A Kryzhanovskii
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引用次数: 0

摘要

在酒精性心肌病模型上,研究慢性乙醇消耗和保温应激对离体大鼠主动脉反应性及主动脉内源性血管收缩受体表达的影响。以10%乙醇溶液为唯一液体来源,对远交种大鼠进行24-28周的推醇处理。在评估研究结果时,考虑到了动物的年龄。研究发现,老龄(40-45周龄)非应激大鼠分离的主动脉环对内皮素-1 (ET1)、去甲肾上腺素(NA)、精氨酸抗利尿素(AVP)或血管紧张素II (ATII)的反应性与幼龄动物的反应性无明显差异。然而,随着预期寿命的增加,血管对5 -羟色胺(5HT)血管收缩作用的敏感性增加。长时间的应力隔离和高剂量乙醇的消耗导致ET1和na诱导的主动脉环收缩增加,主动脉对影响ATII和AVP的收缩反应显著降低。应激和酒精联合应激引起mRNA ETA-R、AT1A-R的减少。大鼠主动脉V1A-R和α 1 -AR mRNA升高。研究发现,应激和酒精中毒动物血管中胞质糖皮质激素受体(GR)的表达水平降低,GR是基因ETA-R、AT1A-R、V1A-R的转录因子。我们认为,应激和酒精中毒大鼠血管对ATII和AVP的反应性降低是其受体在gr依赖机制上表达减少的结果。结果表明,在乙醇的作用下,血管对5HT的反应性选择性降低。这一过程的机制尚不清楚。重要的是,在停止接受乙醇(逐步戒酒)1个月后,大鼠血管收缩特性的变化与饮酒动物的变化相似。因此,在长期摄入乙醇期间,破坏血管张力的神经内分泌调节的重要性具有应激源成分。此外,在这个实验模型中,我们没有收到支持乙醇直接影响高血压发展的数据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Vascular reactivity and receptor expression of endogenous vasoconstrictor in rats with alcoholic cardiomyopathy and insulation stress].

On the model of alcohol cardiomyopathy studied the effect of chronic ethanol consumption and the insulation stress on the reactivity of isolated rat aorta and the expression of the endogenous vasoconstrictor receptors in the aorta. Pushing alcoholization outbred rats was carried out for 24-28 weeks, using as the sole source of liquid 10% ethanol solution. In assessing the results of the study took into account the age of the animals. It is found that the reactivity of isolated aortic rings dissected from the body of old (40-45 weeks) nonstressed rats in response to endothelin-1 (ET1), noradrenaline (NA), arginine vasopressin (AVP) or angiotensin II (ATII) is not different from such reactivity for young animals. However, with the increase in life expectancy increases the sensitivity of vessels to vasoconstrictor action of serotonin (5HT). Prolonged stress insulation and the consumption of high doses of ethanol the stress lead to increased ET1- and NA-induced contraction of the aortic rings and a significant decrease in contractile response of the aorta to the impact ATII and AVP. Stress and alco- hol in combination with stress causing reduction mRNA ETA-R, AT1A-R. and V1A-R and increased mRNA α₁-AR in rat aorta. It is found that in the vessels of stressed and alcoholized animals reduced level of expression of cytosolic glucocorticoid receptors (GR), which is a transcription factor for genes ETA-R, AT1A-R V1A-R. It is propoused that the development of vascular hyporesponsiveness of stressed and alcoholized rats to action ATII and AVP is the result of reducing the expression of their receptors on the GR-dependent mechanism. It is shown that under the influence of ethanol vessels become hyporeactivity selectively with respect to the action of 5HT. The mechanism of this process is unclear. Importantly, the changes in the contractile properties vessels recovered from the rat at 1 month after the abolition of the reception of ethanol (step abstinence) were similar to changes found at the alcohohzed animals. Thus, the importance of breaking the neuroendocrine regulation of vascular tone during long-term consumption of ethanol has a stressor components. Furthermore, in this experimental model we not received data in favor ethanol direct impact on the development of hypertension.

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